[Risk factors associated with postnatal depressive symptomatology: a study conducted in the Southern Area of the Local Health Unit of Modena]. / Fattori di rischio associati a sintomi depressivi dopo il parto: un'indagine svolta nell'Area Sud dell'Azienda USL di Modena.

OBJECTIVE: postpartum depression is one of the most important and common health problems. The aim of this study is to investigate and determine significant risk factors associated with the development of postnatal depressive symptomatology at 6-8 weeks after childbirth in a sample of Italian women. DESIGN: retrospective study on risk factors related to the development of postnatal depressive symptomatology at 6-8 weeks after childbirth. SETTING AND PARTICIPANTS: the study was conducted in the Southern Area of the Local Health Unit of Modena: 300 women who gave birth in Pavullo in the Frignano's Hospital or in Sassuolo's Hospital from 13.12.2009 to 3.2.2010 were considered. METHODS: four weeks after delivery, women had to complete the Postpartum Depression Predictors Inventory-Revised (PDPI-R) to detect the presence of specific risk factors. Then a double-test strategy, including the Edinburgh Postnatal Depression Scale (EPDS) and the General Health Questionnaire 12 items (GHQ12) at 6-8 weeks after childbirth, was used. The women who scored values above the cut-off in both tests have been considered to have high depressive symptomatology. RESULTS: risk factors associated with postnatal depressive symptomatology were: low self-esteem, prenatal anxiety, prior depression, child care stress and baby blues (p <0.01), prenatal depression, lack of social support from partner and difficult infant temperament (p <0.05). CONCLUSION: 14.3% of the women considered showed high depressive symptomatology at 6-8 weeks after delivery (according to the prevalence rates of postpartum depression in Western Countries). Furthermore, the results (risk factors) mainly confirmed the evidence of the international literature.

Psychological well-being outcomes in disease-free survivors of mid-low rectal cancer following curative surgery.

OBJECTIVE: The aim of this cross-sectional study was to evaluate psychological well-being outcomes in disease-free survivors who previously underwent radical surgery for rectal adenocarcinoma. METHODS: All patients with rectal adenocarcinoma who underwent primary surgery at a single institution from 1990 to 2002 were considered for inclusion in the study. We identified and sent questionnaires to 145 patients after excluding those who had died or had recurrent disease. One hundred and seventeen patients (men/women: 74/43; median age: 65 years) returned the questionnaires. Patients' well being was evaluated using the Psychological General Well-Being Index (PGWBI) questionnaire. The mean PGWBI score was compared with normative data of the general population. The impact of patient-, tumor- and treatment-related factors on patients' long-term psychological well-being status was also evaluated. RESULTS: Compared with the general population, study patients had significantly better anxiety, depressed mood, positive well being, general health, vitality scales and global index scores. On multivariate analysis, positive well being was independently affected by time from diagnosis (36 months; p=0.025) and occurrence of early major complications (p=0.024). Variables that were independently associated with worse self-control included primary education (p=0.04) and the presence of fecal urgency (p=0.049). General health was negatively affected by time from diagnosis (36 months; p=0.047) and fecal urgency (p=0.009). CONCLUSIONS: Patients who have survived cancer are likely to re-evaluate the importance of everyday events and this may explain why they had better PGWBI scores. This study also identified that a short time from diagnosis, early adverse events and bowel dysfunction had a negative impact on patients' well being.

In vitro astrocyte and cerebral endothelial cell response to electrospun poly(epsilon-caprolactone) mats of different architecture.

This work focuses on the evaluation of the potential use of electrospun poly(epsilon-caprolactone) (PCL) micrometric and/or sub-micrometric fibrous membranes for rat hippocampal astrocyte (HA) and rat cerebro-microvascular endothelial cell (CEC) cultures. Both mats supported cell adhesion, proliferation, cellular phenotype and spreading. Microfibrous mats allowed cellular infiltration, while both HAs and CECs were unable to migrate within the sub-micrometric fibrous mat, leaving an acellularized inner region. This finding was correlated to the presence of larger voids within electrospun PCL microfibrous mats, suggesting that the morphology should be accurately selected for the realization of a cell environment-mimicking mat. Based on our results, the proper fiber architecture can be regarded as a crucial issue to be considered in order to deal with suitable polymeric mats tailored for specific in vitro application.

Microstructure and cytocompatibility of electrospun nanocomposites based on poly(epsilon-caprolactone) and carbon nanostructures.

Carbon nanostructures (CNSs) are attractive and promising nanomaterials for the next generation of tissue engineering scaffolds, especially in neural prosthesis. Optimizing scaffold vascularization may be an important strategy to promote the repair of damaged brain tissue. In this context, the idea was to evaluate the cell response of electrospun nanohybrid scaffolds loaded with CNSs. Fibrous composites based on poly(epsilon-caprolactone) (PCL) and CNSs were fabricated by means of electrospinning technique. High-purity carbon nanofibers (CNFs) and single-wall carbon nanotubes (SWNTs) were studied. A detailed microstructural characterization was performed to evaluate the most favorable experimental conditions for the realization of fibrous PCL/CNS fabrics. Electrospun mats comprised of rather uniform and homogeneous submicrometric fibers were obtained starting from 1:1 v/v mixture of tetrahydrofuran (THF) and N,N dimethylformamide (DMF). In vitro cytocompatibility tests were performed using rat cerebro-microvascular endothelial cells (CECs). Acquired results showed an increased cell viability for PCL/CNS nanocomposites, suggesting these materials as a suitable environment for endothelial cells. These results are indicative of the promising potential of CNS-based nanocomposites in biomedical devices for tissue engineering applications where endothelial functional properties are required.

Involvement of the receptor for advanced glycation-end products (RAGE) in beta-amyloid-induced toxic effects in rat cerebromicrovascular endothelial cells cultured in vitro.

To ascertain whether the potential biological effects of beta amyloid (betaA) on the endothelium are partly mediated by the receptor for advanced glycation-end products (RAGE), we performed a series of experiments which analyzed the effects of the betaA(1-42) peptide on in vitro cerebromicrovascular endothelial cells (CECs). Our results suggest that RAGE is directly responsible for betaA(1-42) actions on CECs, such as its toxic effect on cell survival, viability and angiogenic capability. We observed that a 6-h incubation period exposing CECs to betaA(1-42) increased the extracellular levels of nitrite. Furthermore, the presence of a nitric oxide synthase inhibitor, L-NAME, was able to enhance CEC survival and viability. Immunocytochemical analyses demonstrated that the peptide induced expression of the inducible form of NOS, iNOS, typically synthesized in response to immune/inflammatory stimuli. Upon blocking the interaction of betaA(1-42) and RAGE, we observed significantly decreased levels of NO and suppression of iNOS immunoreactivity. In conclusion, our data suggest the involvement of RAGE, at least partly, in mediating the effects of betaA(1-42) on CECs. In particular, the decrease of in vitro cell viability and functionality and nitrosative stress activation was inhibited by blocking betaA(1-42)-RAGE interaction.

Comparative effects of Abeta(1-42)-Al complex from rat and human amyloid on rat endothelial cell cultures.

Metal ions are widely recognized as a key factor for the conformational changes and aggregation of the Alzheimer's disease amyloid (Abeta). So far Al(3+) has received much less attention than other biometals in terms of interaction with Abeta. Brain endothelial cells have been identified as important regulators of the neuronal microenvironment, including Abeta levels. The purpose of this study is to compare the effects of the complex amyloid (Abeta(1-42))-Al, from human and rat, with the effects produced by metal-free Abeta on rat neuroendothelial cells (NECs). To establish Abeta and Abeta-Al toxicity on NECs, survival, vitality, and angiogenesis are evaluated. Cell survival is reduced by human and rat Abeta in a time-dependent manner. This toxic effect is remarkably pronounced in the presence of human Abeta-Al. Moreover, rat Abeta has anti-angiogenic properties on NECs, and this effect is aggravated dramatically by using both human and rat Abeta-Al complexes. The data and arguments presented herein clearly demonstrate the involvement of Al(3+) in Abeta aggregation and, consequently, increasing endothelial cell toxicity.

Beta amyloid angiogenic activity in vitro and in vivo.

Angiogenesis has been suggested as a direct contributor to Alzheimer's disease (AD) pathology. The major pathological hallmarks of AD are the presence of neurofibrillary tangles and, beta-amyloid plaques associated with activated microglia, astrocytes, degenerating neurons and vascular toxicity. In this study, Abeta1-40 and Abeta1-42 peptides, both components of the senile plaques in AD, were used to study their angiogenic activity in vitro, by using normal human cerebral endothelial cells (HCECs), and in vivo, by using the chick embryo chorioallantoic membrane (CAM) assay. Results showed that both peptides stimulate in vitro endothelial cell proliferation, chemotaxis and morphogenesis in Matrigel. Moreover, by using the aorta ring assay, both peptides stimulated the formation of capillary-like structures. An angiogenic response was induced in the CAM assay, similar to that induced by fibroblast growth factor-2 (FGF-2), a well-known angiogenic cytokine. Overall, these data support the hypothesis that Abeta peptides may contribute to angiogenesis occurring in AD and suggest that limiting the pro-angiogenic activity of Abeta peptides may therefore provide a useful target to control angiogenesis associated to AD and therefore limit the disease progression.

Caspase-8 activation and oxidative stress are involved in the cytotoxic effect of beta-amyloid on rat brain microvascular endothelial cells.

Several studies have demonstrated that cerebrovascular dysfunction and damage play a significant role in the pathogenesis of Alzheimer disease (AD). In fact, beta-amyloid peptides (Abetas), the major component of the senile plaques and cerebrovascular amyloid deposits in AD, were shown to be cytotoxic to endothelial cells. We have recently observed that Abetas exert a toxic effect on neuromicrovascular endothelial cells (NECs) in a time- and concentration-dependent manner, apoptosis playing a pivotal role in this process. Hence, it seemed worthwhile to investigate the Abeta-mediated apoptosis mechanism in NECs. Abetas were found to induce, after a short incubation period, apoptosis throughout caspase-8 activation. Moreover, Abetas elicited a highly significant (p < 0.001) increase in superoxide dismutase (SOD) levels after a 3-h exposure period, while SOD concentration was not affected after a 24-h incubation. The time-dependent increase in SOD concentration is probably correlated with the production of an excess of reactive oxygen species. Collectively, our findings allow us to conclude that: i) Abetas may induce apoptosis via the activation of caspase-8, presumably by cross-linking and activating receptors of the death-receptor family; ii) oxidative stress is possibly involved in the Abeta-induced cytotoxic effect; and iii) these two mechanisms do not act sequentially but, probably, are independent of each other.

Endothelial cells from human cerebral aneurysm and arteriovenous malformation release ET-1 in response to vessel rupture.

Cerebral aneurysms and arteriovenous malformations (AVM) are a common cause of stroke and cerebral hemorrage. Both are often discovered when they rupture, causing subarachnoid hemorrhage (SAH). SAH-induced vasospasm is mediated by enhanced vasoconstriction due to endothelin-1 (ET-1). We investigated whether endothelial cells (ECs) obtained from aneurysm and AVM express phenotypic and genotypic alterations contributing to the development of vasospasm after SAH. We isolated ECs from human AVM and aneurysm and then confirmed their EC origin by polymerase chain reaction and immunocytochemistry with endothelial markers. Experiments were also carried out with human cerebral microvascular and umbilical vein ECs (HCECs and HUVECs respectively) for comparison. We tested EC proliferation ability and microtubule formation in Matrigel at different cell passages. Five aneurysm (3 ruptured, 2 unruptured) and 3 AVM (2 ruptured, 1 unruptured) ECs were tested for ET-1 release in the culture medium. Aneurysm and AVM ECs expressed von Willebrand factor, Adrenomedullin, and exhibited a progressive reduction of proliferation and in vitro angiogenic ability after the V passage. Significantly higher levels of ET-1 have been detected in ECs from ruptured aneurysms and AVMs. We report the first successful isolation and characterization of primary EC lines from human cerebral vascular lesions. Augmented release of ET-1 is correlated with the rupture of the abnormal vessel confirming its role in vasospasm after SAH. Furthermore, ECs obtained from these vascular malformations can be used as an experimental model to study SAH-induced vasoconstriction.

Apolipoprotein-E modulates the cytotoxic effect of beta-amyloid on rat brain endothelium in an isoform-dependent specific manner.

Several studies support the hypothesis that apolipoprotein-E (ApoE) acts as a pathological chaperone protein that promotes the beta-plated sheet conformation of beta-amyloid (Abeta) peptides into amyloid fibers. In vitro evidence is also available that ApoE inhibits the neurotoxic effect of Abeta in an allele-specific manner (E2 > or = E3 > E4). We have recently shown that Abeta peptides exert a time- and concentration-dependent toxic effect on rat neuromicrovascular endothelial cells (NECs), and this study aimed to ascertain whether ApoE isoforms are able to modulate this effect. ApoE2 and ApoE4 decreased and increased, respectively, the cytotoxic effect of Abeta(1-40) and Abeta(1-42) on NECs, as evaluated by their survival and viability rates. The toxic effect of both Abeta peptides and ApoE4 was associated with the rise in the necrosis rate of NECs within a 24-h incubation period. Moreover, ApoE2 prevented and ApoE4 magnified the inhibitory effect of Abeta on the capability of NECs cultured on Matrigel to form a capillary-like network. The opposite effects of ApoE isoforms could be due to their different interactions with the C-terminal domain of Abeta. ApoE2, at variance with ApoE4, is thought to form sodium dodecyl sulphate-stable complexes with Abeta and, as a consequence, it could block the interactions of the non-fibrillar Abeta peptide with the plasma membrane, Abeta peptide aggregation and the ensuing cytotoxicity. Collectively, our findings confirm the view that ApoE plays a relevant role in the pathogenesis of Alzheimer's disease.

Effects of beta-amyloid on rat neuromicrovascular endothelial cells cultured in vitro.

Several studies have shown that beta-amyloid (beta A) deposits are associated with damage of cerebral vessels and that in Alzheimer's disease (AD) beta A peptides are cytotoxic for cerebral endothelial cells (ECs). However, little is known about the mechanisms underlying these effects of beta A peptides. Hence, we have investigated the effects of beta A(1-40) and beta A(1-42) on rat neuromicrovascular ECs (NECs) cultured in vitro. NECs were isolated, plated (1.5x10(4) cells/cm2) on collagen/fibronectin-coated Petri dishes and cultured in EC growth medium MV2. After 24 h of culture, NECs were incubated with beta A(1-40) and beta A(1-42) (10(-9) or 10(-7) M) and cultured for another 3, 24 or 48 h. Cell viability was assayed by either trypan blue exclusion or by measuring redox activity (MTS assay). Cell proliferation was assessed by measuring the incorporation of 5'-bromo-2'-deoxyuridine into DNA, cell apoptosis by TUNEL assay and cell necrosis by evaluating the release of lactate dehydrogenase. The morphology of cultured NECs was examined by transmission electron microscopy. Other NECs were plated (2.5x10(4) cells/cm2) on Matrigel coated-wells and incubated for 18 h in the presence or absence of beta A peptides for in vitro angiogenesis assay. Beta A peptides significantly decreased NEC viability and enhanced cell apoptosis and necrosis rates. NEC proliferation was not significantly affected. The effects were seen after an incubation period of 3 h (and also 24 h in the case of the redox activity) but not 48 h and beta A(1-42) was much more effective in its toxic effects than beta A(1-40). NECs incubated for 24 h with beta A peptides displayed ultrastructural signs of cell degeneration. beta A peptides prevented NECs cultured on Matrigel to form a capillary-like network and image analysis showed that the downloading of dimensional and topological parameters of the meshwork was significant only in the case of the incubation with beta A(1-42). Collectively our findings allow us to conclude that i) beta A peptides exert a marked toxic effect on cultured NECs, which conceivably reduces their in vitro angiogenic activity; ii) beta A(1-42) is the more toxic form, which could suggest its main role in the pathogenesis of cerebral vessel lesions in AD and iii) the maximum toxic action occurs after a short incubation period, which could be explained by assuming that beta A peptides are unable to accumulate in NECs due to their rapid degradation, thereby allowing NECs to fully recover within 48 h.

Apolipoprotein E as vascular risk factor in neurodegenerative dementia.

Apolipoprotein E (ApoE) is the major lipid-carrier protein in the brain, and several studies provided evidence that ApoE epsilon4 allele can be considered a genetic risk factor for vascular diseases. Findings indicate that Alzheimer disease (AD) and vascular dementia (VaD) may have common risk factors and/or pathogenesis, but their interrelationships still need to be clearly defined. Since ApoE4 imparts risk for both hyperlipidemia and AD, it seemed worthwhile to investigate the possible role of ApoE in the pathogenesis of AD and VaD. To this task, we examined in healthy volunteers, and AD and VaD patients: i) the frequency of ApoE isoforms; and ii) the influence of ApoE genotype on serum lipid levels. Our findings suggest that epsilon4 allele is an important risk factor for the development not only of the Alzheimer type, but also of the vascular type of dementia. In contrast, epsilon2 allele could have a protective role in AD dementia. These results confirm the hypothesis that serum ApoE concentration is dependent on ApoE genotype, but do not support the view that it has to be considered a relevant biochemical marker for AD and VaD.

The impact of risk factors of Alzheimer's disease in the Down syndrome.

Down syndrome (DS) patients, after the fourth decade of life, display some neurophatological features of the Alzheimer's disease (AD). Several hypotheses suggested that apoE4 protein, an AD risk factor, might promote amyloid formation by stabilizing an aggregated conformation of the beta amyloid protein (Abeta). This peptide is the major proteinaceous component of the senile plaques either in AD or DS, and it is a proteolytic product of the amyloid precursor protein (APP). Both brain and platelets express three APP transcripts of the apparent molecular weight of 106, 110 and 130 kDa. In DS the Abeta deposits may ensue, at least in part, from the overexpression of the Abeta precursor gene located on chromosome 21. Aims of the present study were to evaluate the frequency of apoE4 isoform in DS population, and to ascertain whether the ratio between the 130 and the 106-110 kDa platelet APP isoforms is lower in DS, as seems to occur in AD patients. ApoE4 frequency was significantly lower in DS when compared to AD patients. E4 allele frequency of older DS patients was about half that of younger ones. The 130 to 106-110 kDa APP isoform ratio was similar in young DS and control subjects, and markedly lower in AD patients. Our results indicate that: i) in DS patients the early, selective accumulation of Abeta peptides is independent of the ApoE genotype, but the allele epsilon4 predisposes to various causes of premature death; and ii) platelet APP isoform abnormalities, which can be observed in AD patients, do not occur in young DS patients, suggesting a different processing of APP platelets in DS with respect to AD.

Effects of cryopreservation and coculture with pancreatic ductal epithelial cells on insulin secretion from human pancreatic islets.

Long-term storage methods, such as cryopreservation and long-term in vitro culture, hinder the therapeutical application of pancreatic islet transplantation, because they decrease islet viability. Pancreatic ductal epithelial cells (DEC) are putative stem cells for islets, which may secrete specific factors supporting islet growth and function. Hence, we studied the effect of coculture with DEC on the viability of fresh and cryopreserved human pancreatic islets. Islets and DEC were isolated from the pancreas of an organ donor, and part of them were cryopreserved. Fresh and cryopreserved-thawed islets were cultured alone or in the presence of DEC for 14 days at 33 degrees C or 37 degrees C. At day 1 and day 14 of culture, insulin secretion was stimulated by two sequential 45-min exposures to low and high glucose concentrations (3.3 and 16.7 mmol/l, respectively). Insulin concentrations were measured by radio-immunoassay, and the ratio between the insulin responses to high and low glucose was calculated (insulin stimulation index, ISI). After 14 days of culture, some fresh islets were processed for scanning electron microscopy (SEM). At day 14, ISI was markedly reduced in both fresh and cryopreserved islets with respect to 1 day cultures. Cryopreservation reduced ISI at day 1 and day 14, but in the latter case only when cultures were maintained at 37 degrees C. Coculture with DEC did not affect ISI of fresh islets at day 1, and enhanced it at day 14, but only at a culture temperature of 33 degrees C. Conversely, coculture raised ISI of cryopreserved islets at both day 1 and day 14, independently of the culture temperature. SEM showed that at day 14 of culture, the morphology of fresh islets displayed the best preservation when cocultured with DEC at 33 degrees C. Our findings confirm that both long-term culture and cryopreservation decrease viability of human pancreatic islets. Moreover, they indicate that coculture of islets with DEC at 33 degrees C represents a valuable tool to improve the survival and functional activity of islets, especially in the case of cryopreserved material.

In vitro culture of rat neuromicrovascular endothelial cells on polymeric scaffolds.

Polyphosphazenes are polymers possessing a skeleton composed of alternating phosphorous and nitrogen atoms, and two side-moieties linked to each phosphorous atom. Polyphosphazenes with amino acid esters as side-moieties are biocompatible and biodegradable polymers. Two polyphosphazenes, poly[bis(ethyl alanate) phosphazene] and poly[(ethyl phenylalanate)0.8(ethyl alanate)0.8(ethyl glycinate)0.4 phosphazene] (PPAGP) were synthesized, and processed to form small fibers. Their ability to support rat neuromicrovascular endothelial cell (EC) adhesion and growth has been studied, using poly(D,L-lactic acid) as reference compound. Scanning electron microscopy revealed that both poly[bis(ethyl alanate) phosphazene] and PPAGP fibers were thinner than poly(D,L-lactic acid) fibers, and possessed a more irregular and porous surface. All polymers increased EC adhesion, compared with polystyrene, but only polyphosphazenes were able to improve EC growth. The highest increase in EC proliferation was induced by PPAGP, which, as revealed by environmental scanning electron microscopy, was also able to induce ECs to arrange into tubular structures. The conclusion is drawn that PPAGP may provide the best scaffold for engineered blood vessels, because it promotes adhesion, growth, and organization of ECs into capillary-like structures.

Relationship between subcutaneous fat distribution and serum lipids and blood pressures in italian men.

The associations of an index of centripetal adipose tissue distribution, based on skinfold thicknesses, with levels of triglycerides, total cholesterol, HDL-cholesterol, LDL-cholesterol, blood pressures, and the body mass index (BMI) were analyzed in 197 male blood donors, 20-59 years of age, who were asymptomatic of diabetes and cardiovascular disease. Serum lipid variables were correlated with the BMI independently of the index of centripetal adipose tissue distribution. After adjustment for age, only triglyceride levels were positively correlated with the index of centripetal subcutaneous fat distribution irrespective of the BMI. Thus in the population studied, subcutaneous fat distribution appears to be a weak correlate of cardiovascular disease risk factors, except for triglycerides. © 1994 Wiley-Liss, Inc.

Tailored PVA/ECM scaffolds for cartilage regeneration.

Articular cartilage lesions are a particular challenge for regenerative medicine due to cartilage low self-ability repair in case of damage. Hence, a significant goal of musculoskeletal tissue engineering is the development of suitable structures in virtue of their matrix composition and biomechanical properties. The objective of our study was to design in vitro a supporting structure for autologous chondrocyte growth. We realized a biohybrid composite scaffold combining a novel and nonspecific extracellular matrix (ECM), which is decellularized Wharton's jelly ECM, with the biomechanical properties of the synthetic hydrogel polyvinyl alcohol (PVA). Wharton's jelly ECM was tested for its ability in promoting scaffold colonization by chondrocytes and compared with polyvinyl alcohol itself and the more specific decellularized cartilage matrix. Our preliminary evidences highlighted the chance of using Wharton's jelly ECM in combination with PVA hydrogels as an innovative and easily available scaffold for cartilage restoration.

Electrospun tubular scaffolds: on the effectiveness of blending poly(ε-caprolactone) with poly(3-hydroxybutyrate-co-3-hydroxyvalerate).

Tissue engineering can effectively contribute to the development of novel vascular prostheses aimed to overcome the well-known drawbacks of small-diameter grafts. To date, poly(ε-caprolactone) (PCL), a bioresorbable synthetic poly(α-hydroxyester), is considered one of the most promising materials for vascular tissue engineering. In this work, the potential advantage of intimate blending soft PCL and hard poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBV), a polymer of microbial origin, has been evaluated. Nonwoven mats and small-diameter tubular scaffolds of PCL, PHBV, and PCL/PHBV were fabricated by means of electrospinning technique. Mechanical properties and suture retention strength were investigated according to the international standard for cardiovascular implants. Biological tests demonstrated that both PCL-based scaffolds supported survival and growth of rat cerebral endothelial cells in a short time. The fiber alignment of the electrospun tubular scaffolds contributed to a more rapid and homogeneous cell colonization of the luminal surface.

Structural characterization and cell response evaluation of electrospun PCL membranes: micrometric versus submicrometric fibers.

Electrospinning is a valuable technique to fabricate fibrous scaffolds for tissue engineering. The typical nonwoven architecture allows cell adhesion and proliferation, and supports diffusion of nutrients and waste products. Poly(epsilon-caprolactone) (PCL) electrospun membranes were produced starting from 14% w/v solutions in (a) mixture 1:1 tetrahydrofuran and N,N-dimethylformamide and (b) chloroform. Matrices made up of randomly arranged uniform fibers free of beads were obtained. The average fiber diameters were (a) 0.8 +/- 0.2 microm and (b) 3.6 +/- 0.8 microm. PCL matrices showed the following tensile mechanical properties: tensile modulus (a) 5.0 +/- 0.7 MPa (b) 6.4 +/- 0.2 MPa, yield stress (a) 0.55 +/- 0.06 MPa (b) 0.43 +/- 0.02 MPa, and ultimate tensile stress (a) 1.7 +/- 0.2 MPa and (b) 0.8 +/- 0.1 MPa. The ultimate strain ranged between 300% and 400%. Cytotoxicity of electrospun membranes was continuously evaluated by means of electric cell-substrate impedance sensing technique using human umbilical vein endothelial cells (HUVEC). PCL matrices resulted free of toxic amounts of contaminants and/or process by-products. In vitro studies performed by culturing HUVEC on micrometric and submicrometric fibrous mats showed that both structures supported cell adhesion and spreading. However, cells cultured on the micrometric network showed higher vitality and improved interaction with the polymeric fibers, suggesting an increased ability to promote cell colonization.

A cross-sectional study of homocysteine-, NO-levels, and CT-findings in Alzheimer dementia, vascular dementia and controls.

Repetitive measurement with neuroimaging techniques could be useful instruments permitting to differentiate between Alzheimer disease (AD) and vascular dementia (VD). The major genetic risk factor for the development of late-onset AD is the allele epsilon4 of the apolipoprotein E (ApoE). Moreover nitric oxide (NO) and homocysteine (Hcy) seems to be correlated with the degree of cognitive impairment in demented subjects. The aim of this study was to investigate the association between serum NO and Hcy levels, global brain atrophy and brain vascular lesion in AD and VD patients. We report that high plasma levels of homocysteine resulted associated with AD and VD, suggesting that in AD elevated plasma Hcy might be a consequence of concomitant vascular dementia. Otherwise, plasma NO levels were not significantly different in any of the groups. Moreover, neuroimaging measures of vascular lesion level could be of usefulness to differentiate between AD and VD.